Gamma-hydroxybutyric acid (GHB) is a naturally occurring metabolite of GABA which has the ability to produce petit mal-like seizures when administered to animals. We have characterized the biochemical and neurophysiologic ontogeny of this compound, identified specific binding sites for GHB in brain, investigated metabolic sources for GHB in brain other than GABA, and shown that GABAergic mechanisms may play a role in GHB-induced seizures while dopaminergic and cholinergic mechanisms do not. We propose to continue these various lines of investigation into the function of GHB in brain and the mechanism by which it produes petit mal-like seizures. There are three hypotheses to be tested. First that GHB-induced hypothermia is responsible for part or all of the EEG effects of this compound. Second that GABAergic mechanisms play a role in the genesis of GHB-induced seizure. The third hypotheses is that there is a source for GHB in brain additional to GABA. The relation of GHB seizures to GHB-induced hypothermia will therefore be determined. GABA-GHB interaction will be exmained by detail neurophysiologic and ontogeny studies of GABA agonists and GHB as well as by receptor binding studies designed to characterize GHB-GABA interaction at the level of the receptor. The relation of GHB to a possible non-GABA precursor, 1,4 butanediol will be characterized by gas chromatographic/mass spectroscopic techniques.